That the disulfide-metabolizing enzyme, GSH insulin transhydrogenase, (GIT) acting on IgG can modify its structure and cause it to become antigenic in a homologous species will be investigated. Native IgG is not a substrate for GIT and consequently various treatments such as limited proteolysisto make its disulfide bonds accessible to GIT will be sought. Proteins for this purpose will be prepared from leukocytes. It is suggexted that alteration of IgG in the manner described plays a role in the etiology of rheumatoid arthritis.